DDIT3

(redirected from CHOP10)

DDIT3

A gene on chromosome 12q13.1-q13.2 that encodes a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors, which form heterodimers with other C/EBP members—e.g., C/EBP and LAP—preventing their DNA binding activity. DDIT3 is activated by endoplasmic reticulum stress, and plays roles in adipogenesis, erythropoiesis and apoptosis.
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Association between arsenic suppression of adipogenesis and induction of CHOP10 via the endoplasmic reticulum stress response.
The expression of CHOP10 is down-regulated along with the adipogenic hormone challenge, resulting in transactivation of C/EBP[beta].
Antibodies for C/EBP[beta] (sc-61; 1:500), C/EBP[beta] (sc-7962; 1:500), CHOP10 (sc-575; 1:500), and glyceraldehyde 3-phosphate dehydrogenase (GAPDH, sc-20357; 1:500) were obtained from Santa Cruz Inc.
Upon exposure to adipogenic signals, such as DMI or DMIRI cocktail, C/EBP[beta] and C/EBP[delta] are rapidly expressed and transcriptionally regulate the expression of PPAR[gamma] and C/EBP[alpha], whereas C/EBP[euro] and CHOP10 serve as negative regulators of PPAR[gamma] transcription (Batchvarova et al.
To investigate whether UPR, especially CHOP10 induction, is involved in the suppression of terminal adipogenesis by [iAs.
CHOP10 induction in adipogenic suppression by arsenic.
Although the expression of C/EBP[alpha] rises quickly in preadipocytes in response to adipogenic hormones, its DNA-binding activity is initially suppressed through binding with CHOP10 (Tang and Lane 2000).
Among the genes that are transcriptionally regulated by ATF4, ATF6, and XBP1, CHOP10 is one of the mostly expressed inducible genes during ER stress (Oyadomari and Mori 2004).
3+] trigger UPR and induce CHOP10, a protein that inhibits C/EBP[beta] transcriptional activity, thus impairing adipogenesis.
Induction of CHOP10 by arsenic is associated with reduced DNA-binding activity of CCAAT/enhancer-binding protein [beta] (C/EBP[beta]), which regulates the transcription of peroxisome proliferator-activated receptor [gamma] and C/EBP[alpha].
3+] trigger the ER stress response and up-regulate CHOP10, which inhibits C/EBP[beta] transcriptional activity, thus suppressing adipogenesis.